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Viral Immunol. 2007 Spring;20(1):142-9.

Using interferon-alpha to block expression of cellular ribosome subunit S24 variant 2 in human fibroblasts inhibits translation of the poliovirus genome.

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  • 1Institute of Medical Biology, Chinese Academy of Medical Sciences, Peking Union Medical College, Kunming, People's Republic of China.


Studies about the proteins induced by interferon (IFN-)-alpha stimulation have provided some data on their mechanism of antiviral effect. These proteins were confirmed to contribute to antiviral functions. In this study, IFN-alpha stimulation of human fibroblasts was shown to induce the inhibition of S24 variant 2 (a structural component of the ribosomal small subunit) at the mRNA and protein levels, implying a possible antiviral mechanism for IFN-alpha in human fibroblasts. The delay of poliovirus replication by IFN-alpha was partially compensated for by S24 variant 2 expressed in pcDNA vector-transfected cells, and the interference RNA of S24 variant 2 was able to induce mimetically, to some extent, this poliovirus replication delay. These observations revealed that S24 variant 2 could be involved in the antiviral effects of IFN-alpha in human fibroblasts.

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